The possible alteration of biochemical characteristics of various cellular components involved with the excitation-contraction coupling processes is being investigated. The primary objective of the present study is to locate the possible site of defects in cardiac failure in the above coupling processes. In view of the importance of Ca ions in playing one of the critical roles as a regulator of cardiac contractile strength, special emphasis is placed on the investigation of Ca ions movement in cardiac muscle cells during contractile activity. The cardiac failure is produced in rabbits and dogs by surgical constriction of aorta. It was found that the Na ion -K ion activated ATPase of cardiac membrane fragments was unchanged in failed hearts compared to normal. The active Ca ions uptake of sarcoplasmic reticulum of failed hearts was found to be depressed but the active Ca ions transport of mitochondria was rather increased in experimentally induced failed heart. It is proposed to study the Ca ions binding properties of modulatory proteins (troponin and tropomyosin system), in failed hearts. Since it is known that troponin is the CA ions receptor of modulatory proteins, initially the ion binding to troponin in failed hearts will be investigated. Results obtained in failed hearts will be compared with those of normal hearts. Also the interaction of Ca ions to the troponin-tropomysin complex will be investigated during the development of failure. BIBLIOGRAPHIC REFERENCE: Phosphorylation of the red blood cell membrane during the active transport of Ca ions. Y.N. Cha and K.S. Lee. J. Gen. Physiol. 67: 251-261, 1976.